11 10/6/2015 Hypersensitive Reactions Allergies Hugh B. Fackrell.

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Transcript of 11 10/6/2015 Hypersensitive Reactions Allergies Hugh B. Fackrell.

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Hypersensitive ReactionsAllergies

Hugh B. Fackrell

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Hypersensitive Reactions Assigned Reading Content Outline Performance Objectives

– Key terms– Key Concepts

Short Answer Questions

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Assigned Reading Chapter: 17 pp 413-439 Janis Kuby’s Immunology 3rd Ed

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Content OutlineGell & Coombs Classification

Type I Hypersensitivity: IgE mediatiated Type II Hypersensitivity: Antibody mediated

cytotoxic Type III Hypersensitivity: Complex mediated

cytotoxic Type IV Hypersensitivity: DTH mediated

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Type I Hypersensitivity: IgE mediatiated

Components Mechanisms Mediators Consequences Regulation Detection Therapy

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Components Allergens IgE Mast cells & basophils IgE binding receptors

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House dust mite Mite fecal pellets are the major

source of the allergen in house dust

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Cat Hair Major cause of allergies

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Type I Hypersensitivity

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Mechanisms receptor cross linkage Intracellular events

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Mechanism of Latex Allergy

3 step process sensitization Activation of mast cells Prolonged immune activity

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Sensitization to Latex Proteins

Macrophage presents Ag to T cells T cells activate B cells via IL-4 B cells become plasma cells make IgE IgE attaches to mast cell receptors

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Activation of Mast cells Allergen binds to IgE on mast cell Intracellular enzyme cascade

– immediate release of histamines cytokines

Induction of intracellular lipids– Prostoglandins, arachadonic acid

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Chemical released by activated mast cells induce basophils and other cells in the bloodstream to migrate into the tissue. These cells sustain immune activity which leads to tissue damage

Prolongation of Immune Activity

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Allergen Activation

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Mediators histamine leukotriens & prostoglandins cytokines

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Consequences systemic anaphylaxis localized anaphylaxis late phase reaction

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Atopic Eczema

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Anaphylatic Response to Bee venom

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Early vs late Response

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Detection

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Skin Patch Test

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Latex QuestionairePositive History

RAST positive Avoid latex Rast Negative Patch tests Positive

Identify allergen Patch tests

NegativeTreat dermatitis

Negative History RAST positive Latex test positive

Avoid latex latex test negative powder free

gloves Rast negative

Safe to use latex

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Therapy Hyposensitization

– IgG as blocking antibody»repeated subcutaneous injections

– T cell anergy»soluble antigens

Antihistamines

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Drugs for Type I hypersenstivity

Antihistamines blocks receptors Cromolyn sodium blocks Ca++ influx Theophylline

– inhibits phosphodiesterase– [cAMP] kept high

Epinephrine– stimulates cAMP via beta adrenergic receptors

Cortisone – blocks conversion of histidine to histamine

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Performance Objectives

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Key Terms allergen, allergy, anaphylactic

shock,anaphylaxis, anergy, atopy, basophils,

contact sensitivity, degranulation, delayed type hypersensitivity,

desenstization, granulomas, homocytotropic antibodies, hypersensitivity,

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hyposensitivity, immediate hypersensitivity, late phase reaction, mast cells,

sensitization, senstizing dose, shocking dose, systemic anaphlyaxis, triple response: edema, erythema, wheal and flare,

tubercles, tuberculin skine reaction, tuberculosis, Type I hypersensitivity,

Type II hypersensitivity, Type II hypersensitivity, Type IV hypersensitivity.

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Key Concepts List the Gell & Coombs classification for

hypersensitivity reactions; give examples of each type.

Describe stimulatory hypersensitivity and give a specific example

Discuss the difference between primary and secondary exposure to antigen in imunity and in hypersensitivity

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Describe the structural and functional characteristics of IgE.

Discuss the cytotropic nature of IgE

Differentiate betweeen the cyclooxygenase and lipoxygenase pathways of mediator production

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Describe the role of mast cells in immediate hypersensitivity reactions.

Distinguish between release of preformed and newly formed mediators from mast cells and give examples of each type of mediator

Discuss the hallmarks of delayed type hypersensitivity

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Explain the mechanisms of Delayed Type Hypersensitivity induction and development

Distinguish between different types of Delayed type hypersensitivity.

Describe tuberculosis in terms of hypersensitivity reactions.

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Short Answer Questions

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By derivation, what does allergy mean and what does hypersensitivity mean? Are they synonymous?

The main difference between immediate and delayed types of hypersensivitiy is the time of appearance of the reactions. True/False? If false, name the main differences.

What is the type II reaction described by Gell & Cooombs? Does this reaction require complement?

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Is there a tendency to immediate hypersenstivity reactions? Explain?

Differentiate between antigen and allergen.

What immune and nonimmune cells are involved in immediate hypersensivity?

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What class of antibody in responsible for immediate hypersenstivity? Describe some structural and biological characteristics of this antibody?

What do we mean by homocytotropic antibodies?

Briefly describe the result of the interaction of IgE, with mast cells– a) in the presence of allergen.– b) in the absence of allergen.

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What are the chemical mediators of immediate hypersentivity reactions?

Some effector molecules of immediate hypersensitivity reactions are preformed mediators; others are newly synthesized mediators. Distinguish between the two.

Briefly describe the two pathways for the production of newly synthesized mediators.

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How can you determine whether a person is allergic to a foreign protein?

What is the triple response? Name two "in vitro" tests.

What is the mechanism for desensitization for immediate hypersensitivities? Is this desensitization lifelong? If not speculate on the reasons. What are some other modes of treatment for immediate hypersensitivity?

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Describe the differences between systemic anahylaxis and atopy?

Are the mechanisms of cell-mediated immunity and DTH the same?

Name the effector cells in DTH. What are some of the hallmarks of

DTH reactions?

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Describe contact sensitivity. How does contact sensitivity differ

from the tuberculin skin reaction? What is the mechanism of the

tuberculin skin test? If the test is positive what causes the induration (hardening) of the test site? What substances are used in this test?

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DONE!!!DONE!!!